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J Thorac Cardiovasc Surg 2002;124:821-827
© 2002 The American Association for Thoracic Surgery
Surgery for Congenital Heart Disease (CHD) |
From the Divisions of Cardiologya and Cardiothoracic Surgeryb and the Departments of Pediatrics and Surgery, The Children's Hospital of Philadelphia and The University of Pennsylvania School of Medicine, Philadelphia, Pa.
Presented in part at the 74th Annual Meeting of the American Heart Association, Anaheim, Calif, November 14, 2001.
Received for publication Nov 2, 2001. Revisions requested Dec 13, 2001; revisions received Jan 8, 2002. Accepted for publication Feb 10, 2002. Address for reprints: Mitchell I. Cohen, MD, Division of Pediatric Cardiology, The Children's Hospital of Philadelphia, 34th & Civic Center Blvd, Philadelphia, PA 19104 (E-mail: cohenmi{at}email.chop.edu).
Objective: We sought to evaluate possible predictors of early and late pacemaker infections in children.
Methods: A review was performed of all pacemakers implanted in children at The Children's Hospital of Philadelphia between 1982 and 2001. Infections were classified as superficial cellulitus, deep pacemaker pocket infection necessitating removal, or positive blood culture without an identifiable source.
Results: A total of 385 pacemakers (224 epicardial and 161 endocardial) were implanted in 267 patients at 8.4 ± 6.2 years. All 2141 outpatient visits were reviewed (median follow-up, 29.4 months; range, 2-232 months). There were 30 (7.8%) pacemaker infections: 19 (4.9%) superficial infections; 9 (2.3%) pocket infections; and 2 (0.5%) isolated positive blood cultures. All superficial infections resolved with intravenous antibiotics. The median time from implantation to infection was 16 days (range, 2 days-5 years). Only 1 deep infection occurred after primary pacemaker implantation. Six patients with deep infections were pacemaker dependent and were successfully managed with intravenous antibiotics, followed by lead-generator removal and implantation of a new pacemaker in a remote location. In univariate analyses trisomy 21 (relative risk, 3.9; P < .01), pacemaker revisions (relative risk, 2.5; P < .01), and single-chamber devices (relative risk, 2.4; P < .05) were identified as predictors of infection. However, in multivariate analyses only trisomy 21 and pacemaker revisions were predictors.
Conclusions: The incidences of superficial and deep pacemaker infections were 4.9% and 2.3%, respectively. Trisomy 21 and pacemaker revisions were significant risk factors in the development of infection after pacemaker implantation. For primary pacemaker implantation, the risk of infection requiring system removal is low (0.3%).
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